ArticleCell cycle (Georgetown, Tex.)2012
Downregulation of Cdc6 and pre-replication complexes in response to methionine stress in breast cancer cells.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Carboxy-Methylation of the Catalytic Subunit of Protein Phosphatase 2A (PP2Ac) Integrates Methionine Availability with Methionine Addicted Cancer Cell Proliferation.Biomolecules · 2025Article
- The role of BCancer & metabolism · 2025Article
- Methionine Restriction Attenuates Scar Formation in Fibroblasts Derived from Patients with Post-Burn Hypertrophic Scar.International journal of molecular sciences · 2025Article
- The Pivotal Role of One-Carbon Metabolism in Neoplastic Progression During the Aging Process.Biomolecules · 2024Review
- Rescue of Methionine Dependence by Cobalamin in a Human Colorectal Cancer Cell Line.Nutrients · 2024Article
- MGL S3 Chimeric Enzyme Drives Apoptotic Death of EGFR-Dependent Cancer Cells through ERK Downregulation.International journal of molecular sciences · 2022Article
- Pancreatic Cancer Research beyond DNA Mutations.Biomolecules · 2022Review
- Reversion of methionine addiction of osteosarcoma cells to methionine independence results in loss of malignancy, modulation of the epithelial-mesenchymal phenotype and alteration of histone-H3 lysine-methylation.Frontiers in oncology · 2022Article
- Targeting the methionine addiction of cancer.American journal of cancer research · 2022Review
- Methylosystem for Cancer Sieging Strategy.Cancers · 2021Review
- Amino acid metabolism as a therapeutic target in cancer: a review.Amino acids · 2021Review
- Sensing and Signaling of Methionine Metabolism.Metabolites · 2021Review
- Lipid remodeling in response to methionine stress in MDA-MBA-468 triple-negative breast cancer cells.Journal of lipid research · 2021Article
- Methionine represses the autophagy of gastric cancer stem cells via promoting the methylation and phosphorylation of RAB37.Cell cycle (Georgetown, Tex.) · 2020Article
- Association between Metabolites and the Risk of Lung Cancer: A Systematic Literature Review and Meta-Analysis of Observational Studies.Metabolites · 2020Review
- Novel Antiproliferative Biphenyl Nicotinamide: NMR Metabolomic Study of its Effect on the MCF-7 Cell in Comparison with Cisplatin and Vinblastine.Molecules (Basel, Switzerland) · 2020Article
- Methionine Dependence of Cancer.Biomolecules · 2020Review
- Interactome analysis of gene expression profiles identifies CDC6 as a potential therapeutic target modified by miR-215-5p in hepatocellular carcinoma.International journal of medical sciences · 2020Article
- Amino acids in cancer.Experimental & molecular medicine · 2020Review
- Isolation and Characterization of Methionine-Independent Clones from Methionine-Dependent Cancer Cells.Methods in molecular biology (Clifton, N.J.) · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Methionine and homocysteine are metabolites in the transmethylation pathway leading to synthesis of the methyl-donor S-adenosylmethionine (SAM). Most cancer cells stop proliferating during methionine stress conditions, when methionine is replaced in the growth media by its immediate metabolic precursor homocysteine (Met-Hcy+). Non-transformed cells proliferate in Met-Hcy+ media, making the methionine metabolic requirement of cancer cells an attractive target for therapy, yet there is relatively little known about the molecular mechanisms governing the methionine stress response in cancer cells. To study this phenomenon in breast cancer cells, we selected methionine-independent-resistant cell lines derived from MDAMB468 breast cancer cells. Resistant cells grew normally in Met-Hcy+ media, whereas their parental MDAMB468 cells rapidly arrest in the G 1 phase. Remarkably, supplementing Met-Hcy+ growth media with S-adenosylmethionine suppressed the cell proliferation defects, indicating that methionine stress is a consequence of SAM limitation rather than low amino acid concentrations. Accordingly, mTORC1 activity, the primary effector responding to amino acid limitation, remained high. However, we found that levels of the replication factor Cdc6 decreased and pre-replication complexes were destabilized in methionine-stressed MDAMB468 but not resistant cells. Our study characterizes metabolite requirements and cell cycle responses that occur during methionine stress in breast cancer cells and helps explain the metabolic uniqueness of cancer cells.
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